Does acute catastrophic psychological stress disrupt diurnal cardiovascular variability?

Does Acute Catastrophic Psychological Stress Disrupt Diurnal Cardiovascular Variability? To the Editor: Prof Parati et al1 reported an interesting case in which ambulatory blood pressure (BP) monitoring was performed at the time of an earthquake (4.7 on Richter scale), which demonstrated than acute catastrophic psychological stress can raise BP and heart rate in an ambulatory setting. In a recent study,2 we investigated earthquake-induced BP elevation in elderly hypertensive outpatients (mean age, 69 years) living near the epicenter of the 1995 Hanshin-Awaji earthquake (7.2 on Richter scale). In this population, in which BP had been measured before the earthquake, clinic systolic and diastolic BP were 14 mm Hg and 6 mm Hg higher during the first 2 weeks after the earthquake while major aftershocks persisted, but returned to baseline by 3 to 5 weeks. There is thus a discrepancy between Dr Parati’s case and our hypertensive patients. In Dr Parati’s case, although pronounced BP variability persisted throughout the following 6 hours, the earthquake-induced BP elevation lasted only 1 hour. In our study,2 the BP elevation varied according to whether the patients had microalbuminuria: in those who did not, BP returned completely to the baseline value 4 weeks after the earthquake, but in those who had microalbuminuria, the BP increase was prolonged for at least 2 months. Microalbuminuria is closely related to endothelial cell dysfunction, and the different time courses in BP recovery after the earthquakes between Parati’s case and our report might be owing to differences in endothelial cell function and to the persistence of aftershocks. Parati’s patient was a young (34-year-old) normotensive (BP 130/ 85 mm Hg) woman without any target organ damage. Even in the absence of target organ damage, acute stress might affect nocturnal BP. Parati’s case seems to show a nondipping pattern from inspection of his figure, and the absence of a nocturnal reduction in heart rate suggests persistent sympathetic activation during the night and poor sleep quality. Our recent studies have suggested that in addition to poor sleep quality,3 psychological factors such as subclinical depression may contribute to nondipping of nocturnal BP.4 This earthquake-induced nondipping status might also be related to the nighttime onset of cardiovascular events. In our previous study of the 6 districts in the Awaji Island near the epicenter, coronary heart disease (myocardial infarction and sudden death within 24 hours) and stroke were increased 1.5-fold and 1.9-fold, respectively, during the 3-month period after the earthquake compared with the same period of the previous year.5,6 This stress-induced increase in cardiovascular events was observed only in the period from midnight to early in the morning, and there was no increase of cardiovascular deaths during the active daytime period, from noon to midnight. And a previous paper7 reporting on the time of onset of acute myocardial infarctions found that 53% of depressed patients compared with 20% of nondepressed patients reported an onset of symptoms between 10:00 PM to 6:00 AM.